Abstract
BackgroundThe association between driver genes and the incidence of thromboembolic events (TEs) in patients diagnosed with non-small-cell lung cancer (NSCLC) needs to be quantified to guide clinical management.MethodsWe interrogated PubMed, Embase, Web of Science and Cochrane library databases for terms related to venous thromboembolism (VTE) and arterial thromboembolism (ATE) in patients diagnosed with non-small-cell lung cancer harboring driver genes. This search was conducted for studies published between 1 January, 2000 and 31 December, 2020. A random-effects meta-analysis was performed to analyze the pooled incidence and odds ratios of VTE in patients with different driver genes.ResultsOf the 2,742 citations identified, a total of 25 studies that included 21,156 patients met eligibility criteria. The overall pooled incidence of VTE in patients with driver genes was 23% (95% CI 18-29). Patients with ROS1 rearrangements had the highest incidence of VTE (37%, 95%CI 23-52). ALK rearrangements were associated with increased VTE risks (OR=2.08,95% CI 1.69-2.55), with the second highest incidence of VTE (27%, 95%CI 20-35). Both groups of patients with EGFR and KRAS mutations did not show a significantly increased risk for VTE (OR=1.33, 95% CI 0.75-2.34; OR=1.31, 95% CI 0.40-4.28).Conclusions ALK rearrangements were shown to be associated with increased VTE risks in patients diagnosed with non-small lung cancer, while there was no significant relation observed between VTE risks and EGFR or KRAS mutations in lung cancer patients.
Highlights
ALK rearrangements were associated with increased Venous thromboembolisms (VTEs) risks (OR=2.08,95% CI 1.69-2.55), with the second highest incidence of VTE (27%, 95%CI 20-35)
ALK rearrangements were shown to be associated with increased VTE risks in patients diagnosed with non-small lung cancer, while there was no significant
Association Between Oncogene and Thromboembolisms relation observed between VTE risks and EGFR or KRAS mutations in lung cancer patients
Summary
Venous thromboembolisms (VTEs), which consist of deep vein thrombosis (DVT) and pulmonary embolisms (PEs), are a common complication associated with cancer, occurring in 510% of cancer patients. Lung cancer has been associated with an intermediate risk of VTE, especially during the first year following cancer diagnosis. The incidence of VTE in lung cancer patients is approximately 7-13% [1, 4]. The aging of the cancer population and the introduction of thrombogenic anti-cancer treatments increase the incidence of VTE in cancer patients [2]. Patients diagnosed with lung cancer are at an increased risk for arterial thromboembolism (ATE), but the impact on the generation of ATE is less severe than that on the generation of VTE [5]. The association between driver genes and the incidence of thromboembolic events (TEs) in patients diagnosed with non-small-cell lung cancer (NSCLC) needs to be quantified to guide clinical management
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